Biology subjects

Zhang, Z. Y.

Publications and source records attributed to Zhang, Z. Y..

3 recordsLinked to original sources

bioRxiv2023

The P2 protein of wheat yellow mosaic virus acts as a VSR to facilitate virus infection in wheat plants

Wheat yellow mosaic virus (WYMV) causes severe viral wheat disease in Asia. The WYMV P1 protein encoded by RNA2 has viral suppressor of RNA silencing (VSR) activity to facilitate virus infection; however, VSR activity has not been identified for P2 protein encoded by RNA2. In this study, P2 protein exhibited strong VSR activity in Nicotiana benthamiana at the four-leaf stage, and point mutants P70A and G230A lost VSR activity. Protein P2 interacted with calmodulin (CaM) protein, a gene-silencing associated protein, while point mutants P70A and G230A did not interact with it. Competitive bimolecular fluorescence complementation and competitive co-immunoprecipitation experiments showed that P2 interfered with the interaction between CaM and calmodulin-binding transcription activator 3 (CAMTA3), but the point mutants P70A and G230A could not. Mechanical inoculation of wheat with in vitro transcripts of WYMV infectious cDNA clone further confirmed that VSR-deficient mutants P70A and G230A decreased WYMV infection in wheat plants compared with the wild type. In addition, RNA silencing, temperature, and autophagy had significant effects on accumulation of P2 protein in N. benthamiana leaves. In conclusion, WYMV P2 plays a VSR role in wheat and promotes virus infection by interfering with calmodulin-related antiviral RNAi defense. One-sentence summaryWYMV P2 protein exerts VSR activity by interfering with the CaM-CAMTA3 interaction to facilitate virus efficient systemic infection in wheat plants.

plant biology↗

bioRxiv2023

The effect of glucagon-like peptide-1 receptor agonist (GLP1RA) on hypertensive-induced heart failure with preserved ejection fraction and hypertensive cardiomyopathy

Emerging preclinical data suggest that glucagon-like peptide-1 receptor agonist (GLP1RA) possesses cardioprotective properties against the pathophysiology of hypertension (HT). We sought to unravel the potential therapeutic application of GLP1RA in a clinically relevant large animal model of hypertensive cardiomyopathy (hCMP). A combination of angiotensin II (Ang II) and deoxycorticosterone acetate (DOCA) pellets were used to induce sustained HT status and establish hCMP in porcine model. Changes in cardiac echocardiography, invasive hemodynamic parameters, neurohumoral biomarkers and inflammation-related cytokines were investigated in 23 adult pigs, among which 6 were serving as control, 9 were induced with HT, and the remaining 8 were HT-induced with GLP1RA treatment. Eight weeks after the study initiated, HT pigs have developed sustained high blood pressure (BP) at both systole and diastole. Phenotype of hCMP has also become significant as impairment in systolic/diastolic function, left ventricular remodeling and cardiac hypertrophy was determined by echocardiogram and invasive hemodynamics. Additionally, blood norepinephrine (NE) content, venoarterial NE gradient and pro-inflammatory cytokines in HT pigs were increased. GLP1RA treatment halted the elevation in BP, left ventricular remodeling and cardiac hypertrophy development; preserved the left ventricular systolic/diastolic function; reduced the venoarterial NE gradient as well as the pro-inflammatory cytokines at 18 weeks in pigs with hCMP. Our results demonstrate that GLP1RA treatment has a remarkable effect on BP decrease, inflammation suppression and left ventricular function improvement. Thus, we provide novel insight into the therapeutic potential of GLP1RA in HT-induced heart failure in a large animal model of hCMP.

physiology↗

bioRxiv2022

Contact Stiffness Governs Mechanoresponses of Living Cells to Extracellular Microenvironment

In interactions between cells and extracellular matrices (ECMs), contact mechanics theory indicates that local ECM deformation depends on both local and non-local forces imposed by cells. In the present study, we investigated the use of a comprehensive variable, contact stiffness (CS), to interpret cell-ECM interactions. CS defines the relationship between the local ECM deformation and the total force from a cell, integrating the effects of individual variables including ECM stiffness, ECM thickness, and cell adhesion area. Through assessments of ECM mechanosensing by human mesenchymal stem cells (hMSCs) under varied CS conditions, we showed that CS scaled well with both yes-associated protein (YAP) activity and the extent of stem cell differentiation. To reveal the cross-scale mechanism underlying mechanosensing, we propose a CS-based motor clutch model, which suggests that various mechanical stimuli affect cells by altering the CS, thus altering the reaction force from the ECM. Using the proposed model, we revealed the contributions of cell architecture evolution to stem cell differentiation and predicted the influence of a non-adjacent ECM layer on cellular mechanosensing. These results demonstrate that the use of CS provides a quantitative predictive framework that allows researchers to address longstanding questions about the effects of ECM mechanics on cell behaviors.

biophysics↗